Department of Biology, Faculty of Science, Istanbul University, 34134 Vezneciler, Istanbul, Turkey.
Neuropeptides. 2011 Apr;45(2):143-50. doi: 10.1016/j.npep.2011.01.001. Epub 2011 Feb 3.
In this study, it was aimed to investigate whether 4-methylcatechol (4-MC) could serve as an autocrine antiapoptotic agent by increasing nerve growth factor (NGF) in β cells of hyperglycemic rats. Rats were divided into four groups: the first group was given citrate buffer and saline, the second group was administered 4-MC, the third group received streptozotocin (STZ), and the fourth group was given both 4-MC and STZ. 4-MC (10 μg/kg) was administered by daily intraperitoneal injection for 10 days before the animals were rendered hyperglycemic by administration of STZ (75 mg/kg). With 4-MC pretreatment on hyperglycemic rats the following results were noted: (i) Increase in plasma glucose, β cell apoptosis and caspase-8 activation was prevented. (ii) Reduction of NGF+ and tyrosine receptor kinase A (TrkA)+ β cell number was blocked. (iii) p75 neurotrophin receptor (p75(NTR))+ β cell number was increased. These data suggest that 4-MC might exert its antiapoptotic actions through NGF/TrkA system which may block NGF/p75(NTR) activation in pancreatic β cells of hyperglycemic rats.
在这项研究中，旨在研究 4-甲基儿茶酚（4-MC）是否可以通过增加高血糖大鼠β细胞中的神经生长因子（NGF）来作为自分泌抗凋亡剂。大鼠分为四组：第一组给予柠檬酸盐缓冲液和生理盐水，第二组给予 4-MC，第三组给予链脲佐菌素（STZ），第四组给予 4-MC 和 STZ。在动物发生高血糖之前，通过给予 STZ（75mg/kg），每天通过腹腔内注射给予 4-MC（10μg/kg）10 天。在高血糖大鼠中用 4-MC 预处理后，注意到以下结果：（i）阻止了血浆葡萄糖，β细胞凋亡和半胱天冬酶-8 激活的增加。（ii）减少了 NGF+和酪氨酸受体激酶 A（TrkA）+β细胞数量。（iii）增加了 p75 神经生长因子受体（p75（NTR））+β细胞数量。这些数据表明，4-MC 可能通过 NGF/TrkA 系统发挥其抗凋亡作用，该系统可能阻止高血糖大鼠胰岛β细胞中 NGF/p75（NTR）的激活。
